Pentagon to Troop-Killing Superbugs: Resistance Is Futile

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Pentagon to Troop-Killing Superbugs: Resistance Is Futile

A super-germ that's become a lethal threat to troops in Iraq and Afghanistan may have met its match in a novel technique that kills entire bacterial colonies within hours.

Today's troops have a nine in 10 chance of surviving their battle injuries. But wounds and amputation sites leave them vulnerable to infection, especially by Acinetobacter – an (opportunistic pathogen) somewhat misleadingly nicknamed "Iraqibacter" for its prevalence in war-zone medical facilities. As Wired magazine reported in 2007, the bacteria has infected at least 700 American troops since 2003, and killed at least seven people exposed to it in military clinics.

Iraqibacter was once treated with common, easy-to-access antibiotic drugs. But in the last few years, the bacteria have developed a powerful resistance to all but one medication, called Colistin, that's got a bit of a nasty side effect: potentially fatal kidney damage.

Since the illness afflicts relatively few people, Big Pharma companies aren't exactly lining up to develop new drugs.

But a Pentagon-funded research team at the University of Massachusetts Amherst, along with small biotech firm PolyMedix, are making rapid strides toward a new line of Iraqibacter treatments – and the medications could spur the development of antibiotics that can fend off other drug-resistant ailments.

"We didn't set out to create a mechanism that could be applied to other illnesses," Dr. Gregory Tew, the UMass scientist behind the project, told Danger Room. "But it's an impressive and exciting bonus that's come of our work."

The scientists have already used the new type of antibiotics to effectively treat staph infections, which kill thousands of Americans each year.

Common antibiotics work by attaching to a specific molecule (like an enzyme) inside bacterial cells. With some minor adaptive changes, bacteria can alter their cell structure to prevent antibiotic binding, thereby becoming resistant to the drugs. Some infections even develop "persister cells," which stop growing when the antibiotics are administered, and then turn back on once a round of meds is completed.

But Tew and his team have developed antibiotics that work from the outside to quickly destroy bacterial cells. The drugs work by poking holes in bacterial membranes, killing the cells instantly. Within a few hours, the antibiotics are able to kill off entire colonies of bacterial pathogens. And resistance is futile: Because the meds don't enter the actual cell, it's impossible for the bacteria to fight back through structural adaptation.

The method has already proven effective in clinical trials for treating staph infections, and the Pentagon is betting it'll be effective in combating Iraqibacter too. In 2009 alone, they doled out nearly $8 million to UMass and PolyMedix, to "study its antibiotic compounds for other biodefense applications and bacterial infections."

Right now, the group is starting animal studies of Iraqibacter antibiotics, though Tew anticipates that human application is several years off. The scientists are also involved in preliminary research on using the membrane-puncture method to address other strains of bacteria.

But a means of mitigating antibiotic-resistant bacteria can't come a moment too soon. Just last month, federal health officials warned that if resistance keeps growing, Americans could soon be living in "a post antibiotic era."